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肌动蛋白α2（ACTA2）下调通过Rho GTP酶激活抑制神经干细胞迁移。

Actin Alpha 2 (ACTA2) Downregulation Inhibits Neural Stem Cell Migration through Rho GTPase Activation.

作者信息

Zhang Ji, Jiang Xuheng, Zhang Chao, Zhong Jun, Fang Xuanyu, Li Huanhuan, Xie Fangke, Huang Xiaofei, Zhang Xiaojun, Hu Quan, Ge Hongfei, Yu Anyong

机构信息

Department of Emergency, Hospital of Zunyi Medical University, 563003 Zunyi, Guizhou, China.

Department of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Military Medical University (Army Medical University), 400038 Chongqing, China.

出版信息

Stem Cells Int. 2020 May 16;2020:4764012. doi: 10.1155/2020/4764012. eCollection 2020.

DOI:10.1155/2020/4764012
PMID:32508931
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7246394/
Abstract

Although neural stem cells (NSCs) could migrate towards lesions after central nervous system (CNS) injury, the migration ability always is restricted due to the disturbed composition and density of the adhesion ligands and extracellular matrix (ECM) gradient after CNS injury. To date, various methods have been developed to enhance NSC migration and a number of factors, which are affecting NSC migration potential, have been identified. Here, primary NSCs were cultured and the expression of actin alpha 2 (ACTA2) in NSCs was determined using reverse transcription polymerase chain reaction (RT-PCR) and immunostaining. Next, the role of ACTA2 in regulating NSC migration and the potential mechanism was explored. Our results demonstrated that ACTA2 expressed in NSCs. Meanwhile, downregulated ACTA2 using siRNA inhibited NSC migration through hindering actin filament polymerization via increasing RhoA expression and decreasing Rac1 expression. The present study might enrich the basic knowledge of ACTA2 in NSC migration and open an avenue for enhancing NSC migration potential, subsequently providing an intervention target for functional recovery after CNS injury.

摘要

尽管神经干细胞（NSCs）在中枢神经系统（CNS）损伤后能够向损伤部位迁移，但由于CNS损伤后黏附配体和细胞外基质（ECM）梯度的组成和密度紊乱，其迁移能力总是受到限制。迄今为止，已经开发了各种方法来增强NSC迁移，并且已经确定了许多影响NSC迁移潜能的因素。在此，培养原代NSCs，并使用逆转录聚合酶链反应（RT-PCR）和免疫染色来测定NSCs中肌动蛋白α2（ACTA2）的表达。接下来，探讨了ACTA2在调节NSC迁移中的作用及其潜在机制。我们的结果表明ACTA2在NSCs中表达。同时，使用小干扰RNA（siRNA）下调ACTA2通过增加RhoA表达和降低Rac1表达来阻碍肌动蛋白丝聚合，从而抑制NSC迁移。本研究可能丰富ACTA2在NSC迁移方面的基础知识，并为增强NSC迁移潜能开辟一条途径，随后为CNS损伤后的功能恢复提供一个干预靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/8629fdaac43a/SCI2020-4764012.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/021d484a243c/SCI2020-4764012.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/15592456ab03/SCI2020-4764012.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/6eb510fdc257/SCI2020-4764012.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/44af963a49e7/SCI2020-4764012.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/918080a7753c/SCI2020-4764012.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/0b7767e60516/SCI2020-4764012.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/8629fdaac43a/SCI2020-4764012.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/021d484a243c/SCI2020-4764012.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/22a2f3f91f49/SCI2020-4764012.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/15592456ab03/SCI2020-4764012.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/6eb510fdc257/SCI2020-4764012.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/44af963a49e7/SCI2020-4764012.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/918080a7753c/SCI2020-4764012.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/0b7767e60516/SCI2020-4764012.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2c0/7246394/8629fdaac43a/SCI2020-4764012.008.jpg

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